The Influence of Aircraft Noise Exposure on Renal Hemodynamic in Healthy Individuals

The World Health Organisation (WHO) estimates that (about 340 million population) 1 million annually health life years are lost by environmental noise exposure in high-income countries of Western Europe. Aircraft noise is thereby assessed at comparable volume as unpleasant as road and rail noise. Epidemiological studies have found a link between aircraft noise exposure and increased incidence of arterial hypertension and thus cardiovascular disease. The underlying pathophysiological mechanisms are not yet fully understood. The kidney acts as a long-term regulator of blood pressure and controls the extracellular sodium and water balance. Significant renal mechanisms of blood pressure regulation are the renin angiotensin system, renal sympathetic activity and sodium excretion. Animal work and clinical studies show that mental stress affects the renal plasma flow and urinary sodium excretion. In spontaneously hypertensive rats environmental stress resulted in sodium retention, triggered by increased renal sympathetic nerve activity, which is the development of arterial hypertension. In a pilot study in subjects at risk for developing arterial hypertension, the investigator observed a lower sodium excretion by mental stress. In healthy volunteers, a 30-minute mental stress test resulted in increased glomerular filtration rate, filtration fraction and an increase in urinary sodium excretion. In the rabbit noise exposure leads to an increase of frequency and amplitude of discharges of renal sympathetic nerve activity and accompanied by a reduction of renal plasma flow. The impact of aircraft noise on renal plasma flow and urinary sodium excretion has, to our knowledge, so far not been studied in humans. In this pilot study the Clinical Research Center investigate the influence of 30 minutes standardized aircraft noise on renal hemodynamics. Hemodynamic renal changes should be considered in the context of the systemic circulation. Therefore, the central hemodynamics is determined in the present pilot study by bioimpedance cardiography.